Coenzyme Q10 supplementation reduces oxidative stress and increases antioxidant enzyme activity in patients with coronary artery disease

Abstract

Objective

The purpose of this study was to investigate the effect of coenzyme Q10 supplementation on oxidative stress and antioxidant enzyme activity in patients with coronary artery disease (CAD).

Methods

This was an intervention study. Patients who were identified by cardiac catheterization as having at least 50% stenosis of one major coronary artery or receiving percutaneous transluminal coronary angioplasty (n = 51) were randomly assigned to the placebo group (n = 14) or one of the two coenzyme Q10-supplemented groups (60 mg/d, n = 19 [Q10-60 group]; 150 mg/d, n = 18 [Q10-150 group]). Intervention was administered for 12 wk. Patients’ blood samples were analyzed every 4 wk for plasma coenzyme Q10 concentrations, malondialdehyde (MDA), and antioxidant enzyme (catalase [CAT], superoxide dismutase [SOD], glutathione peroxidase) activity.

Results

Forty-three subjects with CAD completed intervention study. Plasma coenzyme Q10 concentration increased significantly after coenzyme the Q10-150 intervention (P < 0.01). The MDA levels were significantly lower than baseline in the Q10-150 group at week 4 (P = 0.03). The Q10-150 group had significantly lower MDA levels than the placebo group at week 8 (P = 0.03). With respect to antioxidant enzyme activity, subjects in the Q10-150 group had significantly higher CAT (P = 0.03) and SOD (P = 0.03) activity than the placebo group at week 12. The plasma coenzyme Q10 concentration was significantly correlated with MDA levels (r = −0.35, P = 0.02) and CAT (r = 0.43, P = 0.01) and SOD activity (r = 0.39, P = 0.01). The ratio of plasma coenzyme Q10 to total cholesterol was significantly correlated with SOD activity (r = 0.39, P = 0.02). The ratio of plasma coenzyme Q10 to low-density lipoprotein was significantly correlated with CAT (r = 0.35, P = 0.04) and SOD (r = 0.45, P = 0.01) activity. However, there was no relation between coenzyme Q10 concentration and glutathione peroxidase activity.

Conclusion

Coenzyme Q10 supplements at a dose of 150 mg can decrease oxidative stress and increase antioxidant enzyme activity in patients with CAD. A higher dose of coenzyme Q10 supplements (>150 mg/d) might promote rapid and sustainable antioxidation in patients with CAD.

Introduction

Coenzyme Q10 (also called ubiquinone) is a lipid-soluble benzoquinone with 10 isoprenyl units in the side chain and is a key component of the mitochondrial respiratory chain for adenosine triphosphate synthesis [1], [2]. Coenzyme Q10 is recognized as an intracellular antioxidant that protects membrane phospholipids, mitochondrial membrane protein, and low-density lipoprotein from free radical-induced oxidative damage [3], [4]. Coenzyme Q10 can be synthesized in tissue from farnesyl diphosphate and tyrosine and can be obtained from the consumption of meat, poultry, fish, vegetables and fruits; however, total absorption of coenzyme Q10 from food is thought to be lower than 10% [5], [6].

Cardiovascular disease is the leading cause of death worldwide [7]. Many previous studies [8], [9], [10] have documented a deficiency of coenzyme Q10 in patients with cardiovascular disease and the benefits of treating these patients with coenzyme Q10 supplementation [11], [12], [13], [14], [15]. Additional studies [16], [17], [18], [19] have reported remarkable clinical benefits such as improved tolerance of work in patients with stable angina pectoris after administration of coenzyme Q10 at doses of 30 to 150 mg/d for a short period (1 or 4 wk). A recent study [20] has indicated a relation between low plasma coenzyme Q10 concentration and coronary artery disease (CAD), which may contribute to the higher susceptibility of some individuals to cardiovascular disease, especially Asian Indians and Chinese [21]. A double-blind, randomized, controlled study conducted by Tiano et al. [22] treated 35 patients with ischemic heart disease using coenzyme Q10 at a dose of 100 mg three times daily (300 mg/d) for 1 mo. The results showed a significant increase in the activity of endothelium-bound extracellular superoxide dismutase (SOD) and endothelium-dependent relaxation. Singh et al. [23], [24] suggested that coenzyme Q10 supplements (120 mg/d) administered within 3 d of the onset of symptoms may provide antioxidant protection in patients with myocardial infarction. However, in some clinical trials, coenzyme Q10 supplements produced only a slight improvement or none at all in patients with CAD [25], [26], [27]. The department of health (DOH) in Taiwan recommends a daily intake of no more than 30 mg of coenzyme Q10 for healthy adults but does not provide any information on the use of coenzyme Q10 to prevent CAD. Therefore, in this study we investigated the effect of coenzyme Q10 supplementation (60 and 150 mg/d) on oxidative stress and antioxidant enzyme activity in patients with CAD.